Our data suggest that modulation of ILC3 responses may represent an additional mechanism by which IL-23 may promote tumor formation as we not only observed duodenal IL23A levels to positively correlate with frequencies of mucosal IL-17A-producing ILC3 but also demonstrate IL-23 to trigger expression of the cancer-promoting cytokine IL-17A in duodenal ILC3. The gene discussed is IL17A; the disease is cancer.